Elevated HMGB1 promotes the malignant progression and contributes to cisplatin resistance of non-small cell lung cancer
Abstract Background HMGB1 (high mobility group box B-1) exhibits crucial role in tumor genesis and development, including lung cancer. Whereas, more HMGB1-related details in non-small cell lung cancer (NSCLC) are still largely unclear. Methods The HMGB1 and inflammatory factors in malignant (MPE) an...
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Format: | Article |
Language: | English |
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BMC
2023-07-01
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Series: | Hereditas |
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Online Access: | https://doi.org/10.1186/s41065-023-00294-9 |
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author | Ying Ma Qin Feng Bateer Han Rong Yu Zhiyong Jin |
author_facet | Ying Ma Qin Feng Bateer Han Rong Yu Zhiyong Jin |
author_sort | Ying Ma |
collection | DOAJ |
description | Abstract Background HMGB1 (high mobility group box B-1) exhibits crucial role in tumor genesis and development, including lung cancer. Whereas, more HMGB1-related details in non-small cell lung cancer (NSCLC) are still largely unclear. Methods The HMGB1 and inflammatory factors in malignant (MPE) and non-malignant pleural effusion (BPE) were determined by ELISA. Additionally, qRT-PCR, western blot, or immunohistochemistry were used to determine HMGB1, drug-resistant and apoptotic proteins’ expressions in NSCLC A549, A549-DDP cell lines, and xenograft model. Cell viability, migration/ invasion, and apoptosis were analyzed using MTT, Transwell, and flow cytometry assays, respectively. Results Inflammatory factors and HMGB1 expressions in MPE were significantly higher than BPE of NSCLC. Compared with preoperative and adjacent tissues, significantly higher HMGB1, drug-resistant protein, and anti-apoptotic protein expressions were observed in recurrent tissues. Overexpressed HMGB1 induced NSCLC cells to exhibit stronger aggressive, proliferative, and drug-resistant features. The related abilities were reversed when HMGB1 was interfered. Overexpressed HMGB1 showed a similar co-localization with drug resistant protein P-gp in cytoplasm in xenograft model, while low HMGB1 expression localized in cell nucleus. Conclusions HMGB1 overexpression significantly promoted the malignant progression and cisplatin resistance of NSCLC in vitro and in vivo. |
first_indexed | 2024-03-12T17:08:16Z |
format | Article |
id | doaj.art-6b3d63257d12475ea9c58e4df59ac658 |
institution | Directory Open Access Journal |
issn | 1601-5223 |
language | English |
last_indexed | 2024-03-12T17:08:16Z |
publishDate | 2023-07-01 |
publisher | BMC |
record_format | Article |
series | Hereditas |
spelling | doaj.art-6b3d63257d12475ea9c58e4df59ac6582023-08-06T11:16:29ZengBMCHereditas1601-52232023-07-01160111310.1186/s41065-023-00294-9Elevated HMGB1 promotes the malignant progression and contributes to cisplatin resistance of non-small cell lung cancerYing Ma0Qin Feng1Bateer Han2Rong Yu3Zhiyong Jin4Department of Thoracic Surgery, Affiliated People’s Hospital of Inner Mongolia Medical UniversityInner Mongolia Cancer Hospital and Affiliated People’s Hospital of Inner Mongolia Medical UniversityInner Mongolia Cancer Hospital and Affiliated People’s Hospital of Inner Mongolia Medical UniversityInner Mongolia Cancer Hospital and Affiliated People’s Hospital of Inner Mongolia Medical UniversityDepartment of Thoracic Surgery, Affiliated People’s Hospital of Inner Mongolia Medical UniversityAbstract Background HMGB1 (high mobility group box B-1) exhibits crucial role in tumor genesis and development, including lung cancer. Whereas, more HMGB1-related details in non-small cell lung cancer (NSCLC) are still largely unclear. Methods The HMGB1 and inflammatory factors in malignant (MPE) and non-malignant pleural effusion (BPE) were determined by ELISA. Additionally, qRT-PCR, western blot, or immunohistochemistry were used to determine HMGB1, drug-resistant and apoptotic proteins’ expressions in NSCLC A549, A549-DDP cell lines, and xenograft model. Cell viability, migration/ invasion, and apoptosis were analyzed using MTT, Transwell, and flow cytometry assays, respectively. Results Inflammatory factors and HMGB1 expressions in MPE were significantly higher than BPE of NSCLC. Compared with preoperative and adjacent tissues, significantly higher HMGB1, drug-resistant protein, and anti-apoptotic protein expressions were observed in recurrent tissues. Overexpressed HMGB1 induced NSCLC cells to exhibit stronger aggressive, proliferative, and drug-resistant features. The related abilities were reversed when HMGB1 was interfered. Overexpressed HMGB1 showed a similar co-localization with drug resistant protein P-gp in cytoplasm in xenograft model, while low HMGB1 expression localized in cell nucleus. Conclusions HMGB1 overexpression significantly promoted the malignant progression and cisplatin resistance of NSCLC in vitro and in vivo.https://doi.org/10.1186/s41065-023-00294-9High mobility group B1 (HMGB1)Non-small cell lung cancer (NSCLC)CisplatinMultidrug resistance (MDR) |
spellingShingle | Ying Ma Qin Feng Bateer Han Rong Yu Zhiyong Jin Elevated HMGB1 promotes the malignant progression and contributes to cisplatin resistance of non-small cell lung cancer Hereditas High mobility group B1 (HMGB1) Non-small cell lung cancer (NSCLC) Cisplatin Multidrug resistance (MDR) |
title | Elevated HMGB1 promotes the malignant progression and contributes to cisplatin resistance of non-small cell lung cancer |
title_full | Elevated HMGB1 promotes the malignant progression and contributes to cisplatin resistance of non-small cell lung cancer |
title_fullStr | Elevated HMGB1 promotes the malignant progression and contributes to cisplatin resistance of non-small cell lung cancer |
title_full_unstemmed | Elevated HMGB1 promotes the malignant progression and contributes to cisplatin resistance of non-small cell lung cancer |
title_short | Elevated HMGB1 promotes the malignant progression and contributes to cisplatin resistance of non-small cell lung cancer |
title_sort | elevated hmgb1 promotes the malignant progression and contributes to cisplatin resistance of non small cell lung cancer |
topic | High mobility group B1 (HMGB1) Non-small cell lung cancer (NSCLC) Cisplatin Multidrug resistance (MDR) |
url | https://doi.org/10.1186/s41065-023-00294-9 |
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